Oxidative stress and inflammatory pathways

Oxidative stress and inflammatory pathways represent a complex network of biological processes where an imbalance between reactive oxygen species (ROS) and antioxidant defenses leads to cellular damage and the activation of immune responses. These pathways are intrinsically linked; oxidative stress can trigger inflammatory signaling through the activation of transcription factors like NF-κB, while inflammatory cells release ROS to combat pathogens, often creating a feedback loop that exacerbates tissue injury (Hussain et al., 2016, 'Oxidative stress and inflammation: what are they and why do they matter?'). In chronic diseases, this persistent activation contributes to the pathogenesis of conditions such as atherosclerosis, Alzheimer's disease, and various cancers (NIH, National Institute of Environmental Health Sciences). Therapeutic strategies often focus on neutralizing ROS with antioxidants or inhibiting specific inflammatory mediators like cytokines and prostaglandins. However, because these pathways also play essential roles in normal physiological signaling and host defense, broad inhibition can lead to significant side effects or 'reductive stress' (StatPearls, 'Physiology, Oxidative Stress'). Modern drug development aims for more specific modulation of key nodes within these pathways, such as the Nrf2-Keap1 system or specific inflammasome components, to restore homeostasis without compromising vital functions.

Other names

Redox-inflammatory signalingOxidative-inflammatory axisPro-oxidant and pro-inflammatory cascadesRedox homeostasis and immune signaling

Modulation of redox-sensitive transcription factors (e.g., Nrf2, NF-κB), scavenging of reactive oxygen species (ROS), and inhibition of pro-inflammatory cytokine production and release.